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  • Author: Johanna Kéri x
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Abstract

Acute myeloid leukemia (AML) is a cancerous disease affecting the myeloid line of the bone marrow cells. FLT3, also known as CD135, is a proto-oncogene, which, if mutated, leads to different types of cancer. The protein it encodes presents tyrosine-kinase activity, and its intratandem mutation, FLT3-ITD, leads to uncontrolled proliferation of myeloblasts and worse outcomes in AML patients. There are currently several pharmacological agents that can inhibit the effect of either the proteins with tyrosine-kinase activity or the mutated FLT3 gene. We present the case of a 68-year-old patient, smoker, with a history of arterial hypertension, chronic obstructive pulmonary disease, presenting with headache unresponsive to antalgics, dyspnea after physical exertion, and epistaxis, with onset 2 months prior to his presentation. The patient was diagnosed with AML with positive FTL3 mutation for which conventional induction therapy was initiated. Within the next days, the patient presented several complications related to the disease itself or caused by the treatment, which eventually led to his death.

Abstract

Hematological conditions can lead to serious disturbances in blood rheology, being frequently associated with increased systemic inflammation and increased risk of bleeding. The imbalance between coagulation and thrombolytic factors in patients with acute coronary syndromes may lead to undesirable outcomes, and the success of emergency coronary angioplasty or by-pass grafting may be altered by increased bleeding in coagulopathies such as hemophilia. This paper intends to review the present knowledge in the field of acute coronary syndromes in subjects with hematological and onco-hematological disorders such as thrombotic thrombocytopenic purpura, immune thrombocytopenic purpura, von Willebrand disease, hemophilia, polycythemia vera, erythrocyte disorders, myelodysplastic syndrome, leukemia, lymphoma or myeloma.

Abstract

In Western countries, chronic lymphocytic leukemia (CLL) is one of the most diagnosed leukemia types among elderly patients. CLL is described as an indolent lymphoproliferative disorder, characterized by the presence of a high number of small, mature B-cells in the peripheral blood smear, with a particular immunophenotype (CD5, CD19, CD23 positive and CD20 dim positive) and accumulation in the bone marrow and lymphoid tissue (e.g., lymph nodes, spleen). The experience of the past decades showed that CLL is clinically very heterogeneous; while some patients present a chronic clinical evolution, with a prolonged survival, in which the treatment can be delayed, others suffer from a more aggressive form, which must be treated early and is associated with many relapses. This observation led to several genomic studies that have mapped the genetic modifications involved in the disease conformations, including del(13q14), del(11q), or trisomy 12. On the other hand, certain genetic mutations such as del(17p13)–p53, NOTCH1 mutation, or ZAP70/CD38 increased expression are associated with worse clinical outcome. In order to apply the right treatment strategy, the RAI and BINET staging systems should be considered, which are based on clinical and laboratory assessment, on genetic mutations that may influence the resistance to chemotherapy, as well as the patient’s age and comorbidities. The aim of this manuscript was to present the therapeutic approaches of CLL, in order to attempt to answer the following question: to treat, or not to treat? This clinical update focuses on the managements of CLL patients in the 21st century.

Abstract

Plasma cell leukemia (PCL) is one of the most aggressive monoclonal gammopathies, being characterized by the presence of more than 20% of plasma cells in the peripheral blood and an absolute number of these cells of more than 2×109, with different morphology, from young elements to mature cells. The incidence of PCL varies between 2–4% among multiple myeloma (MM) patients. In comparison with MM, PCL appears more often in younger patients. The following article describes the case of a 49-year-old female patient diagnosed with PCL which needed urgent control of the clinical manifestations due to its irreversible complications. Urgent autologous stem cell transplantation is recommended in this group of patients.

Abstract

Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma (NHL), representing up to 30 percent of all lymphomas. DLBCL is a fast-growing, aggressive form of NHL, which can appear as a transformation from a less aggressive form of lymphoma or can be de novo pathology. The following article describes the case of a 55-year-old female patient who developed a DLBCL as a second malignancy after an R-CHOP-treated marginal zone splenic lymphoma. This was followed by the transformation of the DLBCL into an aggressive acute lymphoblastic leukemia, for which the patient needed aggressive treatment according to the international acute lymphoblastic leukemia protocol.

Abstract

Iron deficiency and anemia affect approximately half of the chronic heart failure patients and they are associated with increased hospitalization rate, lower functional capacity, lower quality of life, and higher mortality. The exact mechanism of iron deficiency in heart failure patients is still not fully understood. Current guidelines recommend ferritin as the most accurate serum biomarker for the diagnosis of iron deficiency. The use of erythropoiesis-stimulating agents is no longer recommended because of the lack of improvement on mortality or hospital readmission rate, and it was associated with a higher rate of thromboembolic events. Intravenous iron replacement therapy is safe and generally well tolerated, with fewer side effects compared to oral administration. Large randomized studies with ferric carboxymaltose demonstrated its effectiveness and superiority to oral administration, and it was associated with a decreased rate of hospitalization rate and worsening heart failure, and improvement of functional capacity and quality of life. Intravenous iron supplementation for chronic heart failure is strongly recommended by European guidelines. Further studies are needed for a better knowledge of this complex pathology and determination of the long-term safety and effectiveness of iron administration in chronic heart failure patients. .

Abstract

Recent studies demonstrated that despite restoration of the sinus rhythm, patients with a positive history of atrial fibrillation (AF) are still at risk of thromboembolic events. The primary objective of this study is to identify new imaging-derived biomarkers provided by modern imaging technologies, such as cardiac computed tomography angiography, delayed enhancement magnetic resonance imaging, or speckle tracking echocardiography, as well as hematological biomarkers, associated with the risk of intracavitary thrombosis in patients with AF, in order to identify the imaging-derived characteristics associated with an increased risk of cardioembolic events. Imaging data collected will be post-processed using advanced techniques of computational modeling, in order to fully characterize the degree of structural remodeling and the amount of atrial fibrosis. The primary endpoint of the study is represented by the rate of thromboembolic events. The rate of cardiovascular death, the rate of major adverse cardiovascular events, and the rate of AF recurrence will also be determined in relation to the degree of structural remodeling and atrial fibrosis.

Abstract

Atrial fibrillation is the most frequent arrhythmia in adults, becoming more frequent with age. Recent clinical studies demonstrated that epicardial fat is linked with atrial fibrillation induction and recurrence. The arrhythmogenic mechanism consists in the fact that the epicardial adipose tissue is metabolically active, inducing local inflammation and enhancing the oxidative stress, which lead to atrial fibrillation as well as atherosclerosis. Having metabolic activity and secreting various anti- and pro-inflammatory biomarkers, the fat surrounding the heart has been linked to the complex process of coronary plaque vulnerabilization. This clinical update aims to summarize the role of epicardial adipose tissue in the pathogenesis, persistence, and severity of atrial fibrillation.